| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 1066936 | Alcohol | 2015 | 8 Pages |
•Prenatal ethanol exposure induces learning and memory defects in female rats.•Cognitive changes coincided with enhanced LTP and depressed depotentiation.•Synaptic plasticity imbalance may be contributed to the cognitive deficits.
Chronic prenatal ethanol exposure (CPEE) can impair long-term potentiation (LTP) in the male hippocampus. Sexually specific alterations were frequently reported in female animals that had been prenatally exposed to ethanol. This study aimed to examine the effects of CPEE on spatial learning and memory, as well as on hippocampal synaptic plasticity in female adolescent rats. Female offspring were selected from dams that had been exposed to 4 g/kg/day of ethanol throughout the gestational period. Subsequently, performance in the Morris water maze (MWM) was determined, while LTP and depotentiation were measured in the hippocampal CA3-CA1 pathway. In the behavioral test, the escape latencies in both initial and reversal training stages were significantly prolonged. Interestingly, LTP was considerably enhanced while depotentiation was significantly depressed. Our results suggest a critical role of synaptic plasticity balance, which may prominently contribute to the cognitive deficits present in CPEE offspring.
